Glyoxal (40% w/w in water)

Glyoxal (40% w/w in water) is an α-oxoaldehyde that inhibits Aldose Reductase, Glutathione Reductase, and NADPH synthase. Glyoxal (40% w/w in water) exhibits cytotoxicity, triggers oxidative stress, induces ROS accumulation, lipid peroxidation, mitochondrial membrane potential collapse, DNA damage, apoptosis, and massive production of advanced glycation end products (AGEs). Glyoxal (40% w/w in water) depletes glutathione and activates MAPK phosphorylation. It has lower toxicity as a fixative than paraformaldehyde (PFA) and serves as a precursor for the synthesis of oxalates and dietary carcinogens. Glyoxal (40% w/w in water) is suitable for research related to calcium oxalate kidney stones, diabetes, atherosclerosis, cardiovascular diseases, retinopathy, and cataracts^{[1][2][3][4][5][6][7]}. In Vitro:Glyoxal (40% w/w in water) drives NAD⁺-dependent glyoxylate production in human liver tissue homogenates and generates oxalate in HepG2 hepatocellular carcinoma cells^[1].
Glyoxal (40% w/w in water) induces concentration- and time-dependent cytotoxicity, lipid peroxidation, and inhibition of its own metabolism in isolated rat hepatocytes^[2].
Glyoxal (1-5 mM; 25-165 min) (40% w/w in water) induces concentration- and time-dependent ROS production in isolated rat hepatocytes^[2].
Glyoxal (0.5-10 mM; 25-135 min) (40% w/w in water) induces concentration-dependent GSH depletion and GSSG production in isolated rat hepatocytes^[2].
Glyoxal (0.5-5 mM) (40% w/w in water) inhibits cytosolic glutathione reductase activity in rat hepatocyte fractions in a concentration- and time-dependent manner in vitro, with an IC₅₀ of 3 mM^[2].
Glyoxal (40% w/w in water)-induced cellular injury, inflammation and oxidative stress can be alleviated by Resveratrol (HY-16561), Luteolin (HY-N0162), morin and Mangiferin (HY-N0290) as well as Clostridium butyricum through regulating immune signaling pathways or cellular detoxification systems, respectively^[4].\n
Glyoxal (0.12 mM; 8 days) (40% w/w in water) reduces glutathione levels and mitochondrial membrane potential, and increases the proportion of oxidized Trx1 in human aortic endothelial cells^[5].
Glyoxal (5-8 mM) (40% w/w in water) induces concentration- and time-dependent collapse of mitochondrial membrane potential in isolated rat hepatocytes^[2].
Glyoxal (1-10 mM; 4-12 h) (40% w/w in water) induces cytotoxicity by reducing mitochondrial activity in bovine pulmonary artery endothelial cells^[6].
Glyoxal (40% w/w in water) exhibits faster penetration efficiency through the cell membrane of COS-7 cells compared with PFA (HY-DY3003). It can rapidly terminate cellular endocytosis, and shows superior performance in terms of cell morphology, cytoplasmic protein cross-linking and nucleic acid fixation. It reduces the half amount of unfixed proteins and maintains the detection signal of RNA fluorescence in situ hybridization^[3].
Glyoxal (40% w/w in water) enhances the fluorescence intensity of STED staining and multiple synaptic/skeletal proteins in rat hippocampal neurons compared with PFA; only the staining signals of LC3B and vimentin are weaker than those with PFA. It is suitable for a variety of cell and tissue samples including cardiac, neural and olfactory epithelial samples. When used for fixation of mouse olfactory epithelium and olfactory bulb, it also yields a higher signal-to-noise ratio for immunostaining^[3].
Glyoxal (40% w/w in water) can be sequestered and bound by aspartame to reduce its free content and block in vitro glycation reactions. Additionally, the glyoxal-induced glycation of human serum albumin can be inhibited by Naringin (HY-N0153), Naringenin (HY-N0100), and Quercetin (HY-18085) via competitive occupation of the binding sites on lysine and arginine residues of the protein^[4].
Glyoxal (40% w/w in water) can be captured and bound by Gallic acid (HY-N0523), Quercetin, glycine, serine, κ-carrageenan, alginic acid and pectin, thereby reducing the content of free Glyoxal in pH 7.0 phosphate buffer, pH 7.4 phosphate buffer, and lysine-glucose model system, respectively^[4].
Glyoxal (GX) (50-200 μM; 8 days) (40% w/w in water) reduces the viability of wild-type and FANC pathway-deficient human aortic endothelial cells, with LD₉₀ values of 0.12 mM and 0.125 mM, respectively^[5].
Glyoxal (0.12 mM) (40% w/w in water) activates the mitogen-activated protein kinase pathway in human aortic endothelial cells, increasing the phosphorylation levels of ERK, JNK and p38 to 105%, 314% and 159% of those in the control group, respectively^[5].
Glyoxal (1-5 mM; 12 h) (40% w/w in water) induces cytotoxicity in bovine pulmonary artery endothelial cells via membrane damage, with significant LDH release observed^[6].
Glyoxal (1 mM; 6-24 h) (40% w/w in water) induces progressive loss of morphology in bovine pulmonary artery endothelial cells^[6].
Glyoxal (1-10 mM; 4-12 h) (40% w/w in water) induces actin cytoskeleton rearrangement in bovine pulmonary artery endothelial cells; induces alterations in tight junctions of bovine pulmonary artery endothelial cells; dose-dependently induces the formation of advanced glycation end products (Amadori products) in bovine pulmonary artery endothelial cells; and almost completely inhibits in vitro angiogenesis of bovine pulmonary artery endothelial cells^[6].
Glyoxal (1-10 mM; 6 h) (40% w/w in water) dose-dependently inhibits DNA synthesis and replication in bovine pulmonary artery endothelial cells^[6].
Glyoxal (1-5 mM; 2-10 h) (40% w/w in water) induces barrier dysfunction in bovine pulmonary artery endothelial cell monolayers in a dose- and time-dependent manner^[6].
Glyoxal (200-800 μM; 1-24 h) (40% w/w in water) induces dose- and time-dependent intracellular acidification, mitochondrial depolarization, morphological damage and apoptosis in E1A-NR3 retinal cells^[7].